Evidence map›Paper›PMID 26273492›Full record

ReviewBone research2013

A Comprehensive Overview of Skeletal Phenotypes Associated with Alterations in Wnt/β-catenin Signaling in Humans and Mice.

Kevin A Maupin, Casey J Droscha, Bart O Williams

Open access · bronzeAbstract readReview
In one paragraph

Review in Bone research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
4.3field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

78 citing papers in PubMed, 140 citations in OpenAlex.

  1. Uncovering phenotypic expansion in AXIN2-related disorders through precision animal modeling.Genetics in medicine : official journal of the American College of Medical Genetics · 2026
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  17. International journal of molecular medicine · 2023
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  18. Multi-Targeting DKK1 and LRP6 Prevents Bone Loss and Improves Fracture Resistance in Multiple Myeloma.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023
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18 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Kevin A MaupinProgram for Skeletal Pathobiology and Center for Tumor Metastasis, Van Andel Research Institute , 333 Bostwick NE, Grand Rapids, MI 49503, USA.
Casey J DroschaProgram for Skeletal Pathobiology and Center for Tumor Metastasis, Van Andel Research Institute , 333 Bostwick NE, Grand Rapids, MI 49503, USA.
Bart O WilliamsProgram for Skeletal Pathobiology and Center for Tumor Metastasis, Van Andel Research Institute , 333 Bostwick NE, Grand Rapids, MI 49503, USA.
Van Andel Institute · US

Funding

Analyzing the Role of Wnt Signaling in Bone DevelopmentR01AR053293 · NIAMS · VAN ANDEL RESEARCH INSTITUTE · PI WILLIAMS, BART O · 2007 to 2016
$4.0M
NIAMS NIH HHS R01 AR053293
6 · The paper itself

Abstract

The Wnt signaling pathway plays key roles in differentiation and development and alterations in this signaling pathway are causally associated with numerous human diseases. While several laboratories were examining roles for Wnt signaling in skeletal development during the 1990s, interest in the pathway rose exponentially when three key papers were published in 2001-2002. One report found that loss of the Wnt co-receptor, Low-density lipoprotein related protein-5 (LRP5), was the underlying genetic cause of the syndrome Osteoporosis pseudoglioma (OPPG). OPPG is characterized by early-onset osteoporosis causing increased susceptibility to debilitating fractures. Shortly thereafter, two groups reported that individuals carrying a specific point mutation in LRP5 (G171V) develop high-bone mass. Subsequent to this, the causative mechanisms for these observations heightened the need to understand the mechanisms by which Wnt signaling controlled bone development and homeostasis and encouraged significant investment from biotechnology and pharmaceutical companies to develop methods to activate Wnt signaling to increase bone mass to treat osteoporosis and other bone disease. In this review, we will briefly summarize the cellular mechanisms underlying Wnt signaling and discuss the observations related to OPPG and the high-bone mass disorders that heightened the appreciation of the role of Wnt signaling in normal bone development and homeostasis. We will then present a comprehensive overview of the core components of the pathway with an emphasis on the phenotypes associated with mice carrying genetically engineered mutations in these genes and clinical observations that further link alterations in the pathway to changes in human bone.

Indexed as

Lrp5/Lrp6mouse modelsskeletal phenotypesWnt signalingβ-catenin

Identifiers

PMID26273492
PMCPMC4472092
OpenAlexW993469591

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.